Male mice were subjected to IRI, fibrosis model. Mice were treated with a mixture of IL-2–IL-2 mAb (IL-2c) and IL-33 (IL-2c/IL-33) for 5 consecutive days, starting from day –3. Samples were harvested and analyzed 28 days after injury. (A) Body weight change graph for the indicated groups. (B) Left kidney weight at termination. (C) Representative images showing H&E, α-SMA, and collagen I staining on kidney sections from sham, PBS, or IL-2c/IL-33–treated mice. Scale bars: 100 μm. (D) Morphometric quantification of α-SMA and collagen I positive staining, from C. (E) qPCR analysis of whole kidneys for the indicated markers of kidney injury Kim1 and Ngal, inflammation (IL-1b) and fibrosis (α-SMA; TNC, tenascin; Vim, vimetin), shown as fold change relative to control samples. Results are a pool of 2 independent experiments; n = 5 for sham; n = 11 for PBS; n = 10 for IL-2c/IL-33. Mean ± SEM. **P < 0.01; ****P < 0.0001 compared with PBS-treated group by 2-tailed Student’s t test.